ASSESSMENT OF MYOCARDIAL INJURY BY SERUM TUMOR-NECROSIS-FACTOR-ALPHA MEASUREMENTS IN ACUTE MYOCARDIAL-INFARCTION

Citation
Mm. Hirschl et al., ASSESSMENT OF MYOCARDIAL INJURY BY SERUM TUMOR-NECROSIS-FACTOR-ALPHA MEASUREMENTS IN ACUTE MYOCARDIAL-INFARCTION, European heart journal, 17(12), 1996, pp. 1852-1859
Citations number
46
Categorie Soggetti
Cardiac & Cardiovascular System
Journal title
ISSN journal
0195668X
Volume
17
Issue
12
Year of publication
1996
Pages
1852 - 1859
Database
ISI
SICI code
0195-668X(1996)17:12<1852:AOMIBS>2.0.ZU;2-9
Abstract
Clinical and experimental data have shown that after acute myocardial infarction there is a significant release of tumour necrosis factor al pha. Therefore, an attempt was made to correlate changes in serum tumo ur necrosis factor alpha concentrations with indices of infarct extent in patients with acute myocardial infarction. In 50 patients with acu te myocardial infarction, blood samples for evaluation of tumour necro sis factor alpha and alpha-hydroxybutyrate-dehydrogenase were collecte d every 6 h until 120 h after admission. Infarct extent was estimated by clinical parameters such as the occurrence of heart failure and rhy thm disturbances, by enzymatic methods such as cumulative release of a lpha-hydroxybutyrate-dehydrogenase and imaging techniques, by late res ting single photon emission tomography -- (201)thallium scintigraphy - - using an extent score and by echocardiography using a wall motion in dex. The maximum change in serum tumour necrosis factor alpha after in farction (Delta TNF) was calculated by subtracting tumour necrosis fac tor alpha concentration on admission from peak tumour necrosis factor alpha concentration. The average peak tumour necrosis factor alpha lev el was observed 84 h after admission (median: 12 pg . ml(-1)). Between the 72nd and the 96th h no significant changes in tumour necrosis fac tor alpha values were observed. Analysis of the data showed that large r Delta(TNF) values were found to be associated significantly with sig ns of heart failure (P=0.003), the presence of rhythm disturbances (P= 0.001), increased enzymatic infarct extent indicated by cumulative rel ease of alpha-hydroxybutyrate-dehydrogenase (r=0.74; P<0.001), large m yocardial perfusion defects measured with (201)thallium scintigraphy ( r=0.80; P<0.001), and a considerable number of left ventricular wall m otion abnormalities (r=0.57; P<0.001). In conclusion, Delta(TNF) is a reliable method of assessing damage severity in the myocardium after a cute myocardial infarction. As only two blood samples are necessary wi thin 84 h, the method may be one of the more convenient for the assess ment of infarct size in clinical practice.